RESUMO
Despite agreement that teaching on professional boundaries is needed, the design of health profession curricula is challenged by a lack of research on how boundaries are maintained and disagreement on where boundaries should be drawn. Curricula constrained by these challenges can leave graduates without formal preparation for practice conditions. Dual role or overlapping relationships are an example: they continue to be taught as boundary crossings amidst mounting evidence that they must be routinely navigated in small, interconnected communities. In this study, we examined how physicians are navigating overlapping personal (non-sexual) and professional relationships with the goal to inform teaching and curricula on professional boundaries. Following constructivist grounded theory methodology, 22 physicians who had returned to their rural, northern and/or remote hometown in British Columbia, Canada or who had lived and practised in a such a community for decades were interviewed in iterative cycles informed by analysis. We identified four strategies described by physicians for regulating multiple roles within overlapping relationships: (a) signalling the appropriate role for the current context; (b) separating roles by redirecting an interaction to an appropriate context; (c) switching roles by pushing the appropriate role forward into the context and pulling other roles into the background; and (d) suspending an interfering role by ending a relationship. Negotiating boundaries within overlapping relationships may involve monitoring role clarity and role alignment, while avoiding role conflict. The enacted role regulation strategies could be critically assessed within teaching discussions on professional boundaries and also analyzed through further ethics research.
RESUMO
Little is known about the deposition and turnover of proteoglycans in liver fibrosis, despite their abundance in the extracellular matrix. Versican plays diverse roles in modulating cell behavior in other fibroproliferative diseases, but remains poorly described in the liver. Hepatic fibrosis was induced by carbon tetrachloride treatment of C57BL/6 mice over 4 weeks followed by recovery over a 28-day period. Primary mouse hepatic stellate cells (HSCs) were activated in culture and versican was transiently knocked down in human (LX2) and mouse HSCs. Expression of versican, A Disintegrin-like and Metalloproteinase with Thrombospondin-1 motifs (ADAMTS)-1, -4, -5, -8, -9, -15, and -20, and markers of fibrogenesis were studied using immunohistochemistry, real-time quantitative PCR, and western blotting. Immunohistochemistry showed increased expression of versican in cirrhotic human livers and the mouse model of fibrosis. Carbon tetrachloride treatment led to significant increases in versican expression and the proteoglycanases ADAMTS-5, -9, -15, and -20, alongside TNF-α, α-smooth muscle actin (α-SMA), collagen-1, and TGF-ß expression. During recovery, expression of many of these genes returned to control levels. However, expression of ADAMTS-5, -8, -9, and -15 showed delayed increases in expression at 28 days of recovery, which corresponded with decreases in versican V0 and V1 cleavage products (G1-DPEAAE(1401) and G1-DPEAAE(441)). Activation of primary HSCs in vitro significantly increased versican, α-SMA, and collagen-1 expression. Transient knockdown of versican in HSCs led to decreases in markers of fibrogenesis and reduced cell proliferation, without inducing apoptosis. Versican expression increases during HSC activation and liver fibrosis, and proteolytic processing occurs during the resolution of fibrosis. Knockdown studies in vitro suggest a possible role of versican in modulating hepatic fibrogenesis.
